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Hyperleptinaemia rather than fasting hyperinsulinaemia is associated with obesity following hypothalamic damage in children

M Shaikh, Endocrinology, Birmingham Children's Hospital, Birmingham, B4 6NH, United Kingdom
R Grundy, Oncology, Birmingham Children's Hospital, Birmingham, United Kingdom
J Kirk, Endocrinology, Birmingham Children's Hospital, Birmingham, United Kingdom

Correspondence: M Guftar Shaikh, Email: guftar.shaikh{at}nhs.net

Abstract

Obesity following hypothalamic damage is often severe and resistant to life-style changes. Disruption of hypothalamic feedback mechanisms which maintain energy homeostasis may be responsible for this intractable obesity. Adipocytokines including Insulin and leptin are also known to be important regulators of appetite and weight.

Objective: To investigate the role of insulin, leptin, adiponectin and resistin in the aetiology of hypothalamic obesity.

Design: This was a cross-sectional study of three groups of children, those with hypothalamic obesity (HO), congenital hypopituitarism (CH) and simple obesity (SO).

Results: A total of 69 children (HO=28, CH=18, SO=23) had leptin, resistin, adiponectin and insulin measured. Although fasting hyperinsulinaemia and insulin resistance was demonstrated, no differences in insulin or insulin resistance were seen between the groups. The HO group, however, had higher levels of leptin, adiponectin and resistin, which persisted even after adjusting for fat mass, compared to the other groups, p<0.05.

Conclusion: No differences in fasting hyperinsulinaemia or insulin resistance were seen between groups, however leptin levels are elevated, even after adjusting for fat mass, suggesting an element of leptin resistance is associated with HO. This is consistent with the inability of leptin to act on the hypothalamus, either due to transport across the blood brain barrier or dysfunctional receptors. The lack of response to leptin may be more important in the development of obesity in these individuals and the fasting hyperinsulinaemia is a result of the increased adipose tissue, rather than the cause of the weight gain.